Modulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria.
O'Hara, Ann M
AffiliationAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland. firstname.lastname@example.org
Enzyme-Linked Immunosorbent Assay
Gene Expression Regulation
MetadataShow full item record
CitationModulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria. 2009, 10:54 BMC Immunol.
AbstractBACKGROUND: Human intestinal epithelial cells (IECs) secrete the chemokine CCL20 in response to infection by various enteropathogenic bacteria or exposure to bacterial flagellin. CCL20 recruits immature dendritic cells and lymphocytes to target sites. Here we investigated IEC responses to various pathogenic and commensal bacteria as well as the modulatory effects of commensal bacteria on pathogen-induced CCL20 secretion. HT-29 human IECs were incubated with commensal bacteria (Bifidobacterium infantis or Lactobacillus salivarius), or with Salmonella typhimurium, its flagellin, Clostridium difficile, Mycobacterium paratuberculosis, or Mycobacterium smegmatis for varying times. In some studies, HT-29 cells were pre-treated with a commensal strain for 2 hr prior to infection or flagellin stimulation. CCL20 and interleukin (IL)-8 secretion and nuclear factor (NF)-kappaB activation were measured using enzyme-linked immunosorbent assays. RESULTS: Compared to untreated cells, S. typhimurium, C. difficile, M. paratuberculosis, and flagellin activated NF-kappaB and stimulated significant secretion of CCL20 and IL-8 by HT-29 cells. Conversely, B. infantis, L. salivarius or M. smegmatis did not activate NF-kappaB or augment CCL20 or IL-8 production. Treatment with B. infantis, but not L. salivarius, dose-dependently inhibited the baseline secretion of CCL20. In cells pre-treated with B. infantis, C. difficile-, S. typhimurium-, and flagellin-induced CCL20 were significantly attenuated. B. infantis did not limit M. Paratuberculosis-induced CCL20 secretion. CONCLUSION: This study is the first to demonstrate that a commensal strain can attenuate CCL20 secretion in HT-29 IECs. Collectively, the data indicate that M. paratuberculosis may mediate mucosal damage and that B. infantis can exert immunomodulatory effects on IECs that mediate host responses to flagellin and flagellated enteric pathogens.
- Functional modulation of human intestinal epithelial cell responses by Bifidobacterium infantis and Lactobacillus salivarius.
- Authors: O'Hara AM, O'Regan P, Fanning A, O'Mahony C, Macsharry J, Lyons A, Bienenstock J, O'Mahony L, Shanahan F
- Issue date: 2006 Jun
- In vitro and ex vivo activation of the TLR5 signaling pathway in intestinal epithelial cells by a commensal Escherichia coli strain.
- Authors: Bambou JC, Giraud A, Menard S, Begue B, Rakotobe S, Heyman M, Taddei F, Cerf-Bensussan N, Gaboriau-Routhiau V
- Issue date: 2004 Oct 8
- Oxidative stress enhances IL-8 and inhibits CCL20 production from intestinal epithelial cells in response to bacterial flagellin.
- Authors: Ivison SM, Wang C, Himmel ME, Sheridan J, Delano J, Mayer ML, Yao Y, Kifayet A, Steiner TS
- Issue date: 2010 Sep
- Flagellin stimulation of intestinal epithelial cells triggers CCL20-mediated migration of dendritic cells.
- Authors: Sierro F, Dubois B, Coste A, Kaiserlian D, Kraehenbuhl JP, Sirard JC
- Issue date: 2001 Nov 20
- Clostridium difficile flagellin stimulates toll-like receptor 5, and toxin B promotes flagellin-induced chemokine production via TLR5.
- Authors: Yoshino Y, Kitazawa T, Ikeda M, Tatsuno K, Yanagimoto S, Okugawa S, Yotsuyanagi H, Ota Y
- Issue date: 2013 Feb 27